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The interaction between FAK, MYCN, p53 and Mdm2 in neuroblastoma

Alicia M Waters, Elizabeth A Beierle1

  • 1University of Alabama at Birmingham, 1600 7th Ave. South, Lowder Room 300, Birmingham, AL 35233, USA. elizabeth.beierle@childrensal.org.

Anti-Cancer Agents in Medicinal Chemistry
|September 18, 2013
PubMed

Insights

Neuroblastoma malignancy stems from dominant cell survival pathways. Targeting focal adhesion kinase (FAK) and its interactions with MYCN, p53, and Mdm2 may reduce tumor growth and offer new therapeutic strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Neuroblastoma tumorigenesis involves dysregulated cell survival pathways, overriding normal apoptosis and senescence.
  • Overexpression of cell survival mechanisms contributes to malignant transformation in neuroblastomas.

Purpose of the Study:

  • To review the role of focal adhesion kinase (FAK) in neuroblastoma.
  • To explore the interactions between FAK, MYCN, p53, and Mdm2 in modulating neuroblastoma growth and malignancy.

Main Methods:

  • Literature review focusing on protein tyrosine kinases and transcription factors in neuroblastoma.
  • Analysis of molecular interactions modulating cell survival pathways.

Main Results:

  • FAK plays a critical role in neuroblastoma cell survival and proliferation.
  • Interactions between FAK, MYCN, p53, and Mdm2 significantly influence tumor malignancy.
  • Dysregulation of these pathways contributes to resistance to apoptosis and senescence.

Conclusions:

  • Targeting FAK and its associated transcription factors presents a potential therapeutic strategy for neuroblastoma.
  • Understanding these molecular interactions is key to developing novel treatments to decrease tumor malignant potential.

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